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Zāles pret HIV var palīdzēt aknu fibrozes ārstēšanā
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03.11.2019


Valensijas Universitātes zinātnieki atklājuši, ka antiretrovīrusu preparāts rilpivirīns (RPV), ko izmanto HIV ārstēšanai, spējīgs samazināt aknu fibrozi. Pētījums publicēts zinātniskajā žurnālā Gut.
Fibroze ir plaša aknu saslimšana, kad aknu audu vietā sāk augt fibrotiskie audi, kam seko ciroze – aknu šūnu vietā stājas stabili saistaudi, un pārmaiņas kļūst neatgriezeniskas, kā rezultātā cilvēka dzīvildze samazinās. Fibroze rodas hronisku aknu slimību un alkohola izraisītu toksisku bojājumu gadījumā. Fibrotisko audu aktīva veidošanās notiek, slimojot ar hepatītu. Jo aknu audus vairāk bojā fibroze, jo sliktāk tās darbojas. Pagaidām vēl nav speciālu zāļu, kas varētu ātri un efektīvi izārstēt patoloģiju. Ārstēšana pacientam ir ilga un smaga.
Taču tagad ļoti iespējams, ka situācija mainīsies uz labāku. Pētījumi parādījuši, ka RPV aktīvi novērš lipīdu uzkrāšanos un izrāda pretošanos un antifibrozu darbību. Zinātnieki turpina klīniskos pētījumus.
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Source: GUT | «Rilpivirine attenuates liver fibrosis through selective STAT1-mediated apoptosis in hepatic stellate cells» | https://gut.bmj.com/content/early/2019/09/17/gutjnl-2019-318372 |
Abstract
Objective
Liver fibrosis constitutes a major health problem worldwide due to its rapidly increasing prevalence and the lack of specific and effective treatments. Growing evidence suggests that signalling through cytokine-activated Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathways regulates liver fibrosis and regeneration. Rilpivirine (RPV) is a widely used anti-HIV drug not reported to produce hepatotoxicity. We aimed to describe the potential hepatoprotective effects of RPV in different models of chronic liver injury, focusing on JAK-STAT signalling regulation.
Design
The effects of RPV on hepatic steatosis, inflammation and fibrogenesis were studied in a nutritional mouse model of non-alcoholic fatty liver disease, carbon tetrachloride-induced fibrosis and bile duct ligation-induced fibrosis. Primary human hepatic stellate cells (hHSC) and human cell lines LX-2 and Hep3B were used to investigate the underlying molecular mechanisms.
Results
RPV exerted a clear anti-inflammatory and antifibrotic effect in all the in vivo models of liver injury employed, and enhanced STAT3-dependent proliferation in hepatocytes and apoptosis in HSC through selective STAT1 activation. These results were reproduced in vitro; RPV undermined STAT3 activation and triggered STAT1-mediated pathways and apoptosis in HSC. Interestingly, this selective pro-apoptotic effect completely disappeared when STAT1 was silenced. Conditioned medium experiments showed that HSC apoptosis activated STAT3 in hepatocytes in an interleukin-6-dependent mechanism.
Conclusion
RPV ameliorates liver fibrosis through selective STAT1-dependent induction of apoptosis in HSC, which exert paracrinal effects in hepatocytes, thus promoting liver regeneration. RPV’s actions may represent an effective strategy to treat chronic liver diseases of different aetiologies and help identify novel therapeutic targets.
View Full Text: http://dx.doi.org/10.1136/gutjnl-2019-318372




 
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